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首页> 外文期刊>Life sciences >Increase in complement component C3 is an early response to experimental magnesium deficiency in rats.
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Increase in complement component C3 is an early response to experimental magnesium deficiency in rats.

机译：补体成分C3的增加是对大鼠实验性镁缺乏的早期反应。

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The importance of the inflammatory process in the pathology of experimental Mg-deficiency has been reconsidered but the sequence of events leading to inflammatory response remains unclear. In this study, the effect of Mg-deficiency on complement system by measuring total C3 concentration, mRNA abundance for rat pre-pro complement C3 in liver by RT-PCR, complement haemolytic activity and C3 activation by Western Blot was studied. Weaning male Wistar rats were fed either Mg-deficient or control experimental diets for 2 or 8 days. At 8 days, a characteristic inflammatory response of Mg-deficiency including hyperaemia, leukocytosis and enlarged spleen was accompanied by an increase in the total C3 quantity in plasma. Moreover, at 8 days, RT-PCR analysis indicated higher level of mRNA rat pre-pro complement C3 in liver from Mg-deficient rats compared to control rats. Even if the inflammatory syndrome was not observed in rats after 2 days, total plasma C3 was shown to be significantly increased as compared to total plasma C3 level in control rats. Because of the high variability of complement haemolytic activity values in Wistar rats, weaning male Sprague-Dawley rats were used in a second experiment. At 8 days, the inflammatory response of Sprague-Dawley rats was accompanied by an increase in total C3 quantity and by a higher haemolytic activity. The Western Blot technique failed to display distinct bands resulting from C3 cleavage in plasma from Mg-deficient rats. Since, the complement C3 is a positive acute phase reactant, the elevation of C3 indicates that the modification of inflammatory response is an early event of Mg-deficiency. However, complement activation does not appear to be involved in the acute phase of the deficiency.
机译：已经重新考虑了炎症过程在实验性镁缺乏症病理中的重要性，但是导致炎症反应的事件顺序仍然不清楚。在这项研究中，研究了镁缺乏对补体系统的影响，方法是通过RT-PCR测量总C3浓度，肝脏中大鼠前原补体C3的mRNA丰度，补体溶血活性和Western Blot活化C3。给断奶的雄性Wistar大鼠饲喂缺镁或对照实验饮食2或8天。在第8天，镁缺乏症的特征性炎症反应包括充血，白血球增多和脾脏肿大，同时血浆中C3总量增加。此外，在8天时，RT-PCR分析表明，与对照大鼠相比，缺镁大鼠的肝脏中mRNA大鼠前原补体C3水平更高。即使在2天后未在大鼠中观察到炎症综合症，与对照组大鼠的总血浆C3水平相比，总血浆C3也显示出显着增加。由于Wistar大鼠补体溶血活性值的高变异性，因此在第二个实验中使用了断奶雄性Sprague-Dawley大鼠。在第8天，Sprague-Dawley大鼠的炎症反应伴随总C3量增加和更高的溶血活性。 Western Blot技术无法显示出缺镁大鼠血浆中C3裂解产生的明显条带。由于补体C3是阳性急性期反应物，因此C3的升高表明炎症反应的改变是镁缺乏的早期事件。然而，补体激活似乎并不参与缺乏的急性期。

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